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High-Fat Diet Promotes Neuronal Loss in the Myenteric Plexus of the Large Intestine in Mice

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Abstract

Background

Obesity is considered a risk factor for other chronic diseases, and diets rich in lipids can cause alterations in the intestinal functions.

Aim

The aim of this study was to investigate the effects of a high-fat diet (HFD) on the myenteric plexus of the large intestine in mice.

Methods

Swiss mice were distributed into four groups: Control animals fed standard chow for 8 and 17 weeks (C8 and C17 groups) and hyperlipidic animals fed HFD for 8 and 17 weeks (Ob8 and Ob17 groups). Immunofluorescence was performed in the large intestine for the morphologic and quantitative analysis of neuronal populations.

Results

Animals in the Ob17 group exhibited increased body weight and visceral fat gain compared with the C17 group. The intestinal area was also reduced in the two Ob groups. In the proximal colon, the Ob17 group exhibited 16.1 % reduction of the general neuronal density and 33 % reduction of the VIP-immunoreactive (IR) subpopulation. The general neuronal density in the distal colon was reduced by 45 % in the Ob17 group, and the nNOS-IR density was reduced by 35 %. The morphometry of neuronal cell bodies in the Ob17 group exhibited a reduction of the neuronal area of all of the neuronal populations studied in the proximal colon, with a reduction of the subpopulations of nNOS-IR and VIP-IR neurons in the distal colon.

Conclusions

The HFD caused neuronal loss in the myenteric plexus, and nitrergic neurons were more resilient. The changes were more pronounced in the distal colon after 17 weeks.

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Acknowledgments

The authors thank the Post-graduation Program in Cell Biology of the State University of Maringá and National Council of Scientific and Technological Development (CNPq) for financial support.

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Correspondence to Nilza Cristina Buttow.

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Beraldi, E.J., Soares, A., Borges, S.C. et al. High-Fat Diet Promotes Neuronal Loss in the Myenteric Plexus of the Large Intestine in Mice. Dig Dis Sci 60, 841–849 (2015). https://doi.org/10.1007/s10620-014-3402-1

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  • DOI: https://doi.org/10.1007/s10620-014-3402-1

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